Sunitinib

製品コードS7781 別名:SU11248

Sunitinib化学構造

分子量(MW):398.47

Sunitinib is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM, and also inhibits c-Kit.

サイズ 価格(税別)  
JPY 16102.00
JPY 32702.00

文献中Selleckの製品使用例(36)

カスタマーフィードバック(14)

  • PDGF-AA induces Ezh2 expression and proliferation in juvenile islets but not in adult islets. Western immunoblots of indicated islet proteins from 3 week or 9 month-old WT islets 2 days after exposure to PDGF-AA alone, or PDGF-AA plus RTK inhibitors Sunitinib.

    Nature 2011 478(7369):349-55. Sunitinib purchased from Selleck.

    Assessment of effects on human juvenile or adult islets after exposure to PDGF-AA (50 ng/ml) for 2 days, with or without Sunitinib (2 uM) or U0126 (10 uM)co-treatment. Average percentage of BrdU+ insulin+ cells was morphometry from sectioned islets immunostained for insulin (green), glucagon (white) and BrdU (red). n = 3-6 independent experiments.

    Nature 2011 478(7369):349-55. Sunitinib purchased from Selleck.

  • Combinational treatment of kinase inhibitors induces the similar phenotype produced by PP1. All images are lateral view with dorsal to the top and anterior to the left. The combinational treatment of Dasatinib (D) or U0126 (U) with Sunitinib (SU),PTK787 (PTK), or ZM323881 (Z) resulted in the shrinkage of dorsal aorta.

    Cell Res 2011 21, 1080-1087. Sunitinib purchased from Selleck.

    Mice harboring PC3 prostate cancer xenograft tumors were treated with vehicle, B20-4.1.1, or sunitinib. Serial sections from tumors were immunostained to measure hypoxia (hypoxyprobe; HP-1) and PIM1 (dashed lines delineate regions of hypoxia).

    Clin Cancer Res, 2018, 24(1):169-180. Sunitinib purchased from Selleck.

  • Western blotting of Mcl-1 in HCT116 cells treated with indicated agents for 24 hours. ABT-263, 5 μmol/L; ABT-737, 5 μmol/L; SAHA, 4 μmol/L; MS-275, 5 μmol/L; regorafenib, 40 μmol/L; sorafenib, 20 μmol/L; UCN-01, 1 μmol/L; sunitinib, 15 μmol/L.

    Cancer Res, 2018, 78(16):4704-4715. Sunitinib purchased from Selleck.

    A, Tumour growth curves from the initial sunitinib drug trials, with endpoint set at 1300 mm3 (mean ± SEM ). Measurements begin one week after tumour inoculation and on the day sunitinib treatment began. Subsequent experimental endpoints were set based on these growth curves and their intersections with this data are shown. B, histogram plot showing the distribution of tumour sizes at day 8 of treatment. Sunitinib treated tumours exceeding 250 mm3 in size were identified as falling into the non-responsive cohort. Sunitinib treatment significantly retards growth of responsive tumours.

    Cancer Res, 2017, 77(4):1008-1020. Sunitinib purchased from Selleck.

  • Sunitinib decreases FLT-3 and RET phosphor ylation but increases ERK phosphorylation in a time-dependent manner. H295R and SW13 cells were treated with sunitinib (10 nM) for various time points as indi-cated. Cell lysates were prepared and phospho-FLT-3, RET, and ERK levels were monitored by Western Blot-ting. Re-probing against FLT-3, RET, and ERK was done to ensure equal protein loading.

    Surgery 2012 152, 1045-50. Sunitinib purchased from Selleck.

    Sunitinib or PD98059 decreases cell proliferation in a dose-dependent manner. H295R and SW13 cells were treated with various concentration of sunitinib or PD98059 for 48 hours as indicated. Treated cells were subjected to the MTS proliferation assay. Similar experiments were repeated 3 times. Histograms represent relative % of OD490 nm absorbance (* P < .05). All data are relative multiples of expression compared with untreated cells. The data are representative of three experiments and are expressed as the mean ?SE.

    Surgery 2012 152, 1045-50. Sunitinib purchased from Selleck.

  • Autophagic activation in sunitinib- and sorafenib- but not AZD6244-treated cells. Medullary thyroid cancer-1.1 (MTC-1.1; A) and TT ( B) cells were treated with dimethyl sulfoxide (DMSO), sunitinib (50 nM), sorafenib (10 nM), AZD6244 (30 nM), or everolimus (20 nM) for 48 hours. Cell lysates were prepared, and light chain 3 (LC3)-I and -II cleaved caspase-3 protein levels were monitored by Western blotting. Reprobing against actin was per formed to ensure equal protein loading. ( C ) MTC-1.1 and TT cells were transiently transfected with autophagy protein 5 (Atg-5) small inter fering RNA. Transfection with scrambled small inter fering RNA was used as a control. After transfection, cells with and without Atg-5 knockdown were exposed to DMSO or 20 nM of everolimus for 48 hours. Cell lysates were pre- pared and LC3-I and -II protein expression levels were monitored by Western blotting. Reprobing against Atg-5 was per formed to monitor Atg-5 knockdown efficiency. Reprobing against actin was per formed to ensure equal protein.

    Surgery 2012 152, 1142-9. Sunitinib purchased from Selleck.

    Autophagy inhibition blocks the antiproliferative effects of sunitinib and sorafenib but not AZD6244. Medullary thyroid cancer–1.1 (MTC-1.1) and TT cells were transfected transiently with scrambled or autophagy protein 5 (Atg-5) small inter fering RNA. After transfection, cells with and without Atg-5 knockdown were exposed to sunitinib (50 nM), sorafenib (10 nM), and AZD6244 (30 nM) for 48 hours. Treated cells were subjected to a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium proliferation assay. Similar experiments were repeated 3 times. Histograms represent the relative percent of OD490 nM absorbance. The asterisk indicates significance versus scrambled small inter fering RNA–treated control ( P < .05). All data are relative multiples of expression compared to untreated cells. The data are representative of 3 experiments and are expressed as the mean ± the standard error.

    Surgery 2012 152, 1142-9. Sunitinib purchased from Selleck.

  • Sunitinib limits the colonial growth of HT-29 by downregulating HIF-1a. (A) The number and size of colonies formed in soft agar. The numbers of small colonies (<50 μm diameter) were not different among conditions of a serial concentration of sunitinib. On the contrary, large colonies (>50 μm diameter) disappeared after incubation with sunitinib. Each point represents the mean and SD from four separate experiments. (B) HIF-1a expression and hypoxia within HT-29 colony. After colonies grew for 4 weeks, HIF-1a and hypoxia were visualized by immunofluoroscence staining. Bar = 20 μm.

    Biochem Bioph Res Co 2010 398, 205-211. Sunitinib purchased from Selleck.

    2. Sunitinib downregulates HIF-1a. (A) Dose-dependent repression of HIF-1a protein level by sunitinib in HT-29. HT-29 cells were incubated under normoxic (N) or hypoxic (H) conditions in the presence of sunitinib for 24 h. HIF-1a and ARNT proteins in total cell lysates were analyzed by Western blotting. (B) Sunitinib attenuates the hypoxic induction of HIF-1 target genes. RNAs were isolated from HT-29 cells subjected to normoxia (N) or hypoxia (H) in the presence of sunitinib for 16 h. The mRNAs of HIF-1a and its target genes were analyzed by RT-PCR and autoradiography. PGK1 indicates phosphoglycerate kinase 1; PDK1, pyruvate dyhydrogenase kinase 1; CAIX, carbonic anhydrase IX. (C) Sunitinib-induced HIF-1 inhibition. Epo-enhancer and b- galactosidase reporter plasmids were co-transfected into HEK293 cells. After 16 h incubation, luciferase and b-galactosidase activities were measured. *P < .05 versus the hypoxic control.

     

     

    Biochem Bioph Res Co 2010 398, 205-211. Sunitinib purchased from Selleck.

  • Sunitinib inhibits 50-UTR-dependent translation of HIF-1a. (A) 50 cap-dependent translational activity of HIF-1a. The luciferase reporter plasmid contains the HIF-1a 50-UTR segment between the tk promoter and the luciferase gene. HT-29 cells were co-transfected with the reporter plasmid (8 lg per 100-mm dish) and the b-gal plasmid (4 μg). After 16 h incubation under normoxic or hypoxic conditions with sunitinib, cells were lysed and subjected to luciferase assay. *P < .05 versus the hypoxic control. (B) IRES-dependent translational activity of HIF-1a. The luciferase reporter plasmid contains the HIF-1a 50-UTR segment between the GFP gene and the luciferase gene. HT-29 cells were co-transfected with the reporter plasmid (8 μg) and the b-gal plasmid (4 μg). *P < .05 versus the hypoxic control. (C) Sunitinib inhibits phosphorylation of Akt. After 8 h incubation under hypoxic condition with sunitinib, HT-29 cells were lysed and subjected to Western blotting. (D) Sunitinib suppresses HIF-1a in VHL-null RCC4 cells. VHL (-/-) RCC4 cells were incubated under normoxic conditions sunitinib for 8 h, and HIF-1a in total cell lysates was analyzed by Western blotting.

     

     

    Biochem Bioph Res Co 2010 398, 205-211. Sunitinib purchased from Selleck.

    Experimental layout for VEGF signaling blocking and LCMV infection in WT mice. Mice received two injections on day 0 and 3 p.i. of Abs as described in Material and Methods, or daily gavage of the VEGFR/PDGFR-inhibitor sunitinib. Inguinal LN volume on day 0 (D0) or day 8 (D8) p.i. after treatment of mice with control Ig or anti-VEGFR2, anti-VEGF-A Abs or sunitinib. Pooled from 1-2 independent experiments with 3-5 mice per treatment. D. Total HEV length on day 0 (D0) or day 8 (D8) p.i. as in C. No significant difference was found in C and D between day 8 control Ig and Ab- or inhibitor-treated values (One-way ANOVA).

    AACR Sunitinib purchased from Selleck.

製品安全説明書

PDGFR阻害剤の選択性比較

生物活性

製品説明 Sunitinib is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM, and also inhibits c-Kit.
ターゲット
FLT3 [1]
(Cell-free assay)
c-Kit [1]
(Cell-free assay)
PDGFRβ [1]
(Cell-free assay)
VEGFR2 [1]
(Cell-free assay)
2 nM 80 nM
体外試験

Sunitinib also potently inhibits Kit and FLT-3. [1] Sunitinib is a potent ATP-competitive inhibitor of VEGFR2 (Flk1) and PDGFRβ with Ki of 9 nM and 8 nM, respectively, displaying >10-fold higher selectivity for VEGFR2 and PDGFR than FGFR-1, EGFR, Cdk2, Met, IGFR-1, Abl, and src. In serum-starved NIH-3T3 cells expressing VEGFR2 or PDGFRβ, Sunitinib inhibits VEGF-dependent VEGFR2 phosphorylation and PDGF-dependent PDGFRβ phosphorylation with IC50 of 10 nM and 10 nM, respectively. Sunitinib inhibits VEGF-induced proliferation of serum-starved HUVECs with IC50 of 40 nM, and inhibits PDGF-induced proliferation of NIH-3T3 cells overexpressing PDGFRβ or PDGFRα with IC50 of 39 nM and 69 nM, respectively. [2] Sunitinib inhibits phosphorylation of wild-type FLT3, FLT3-ITD, and FLT3-Asp835 with IC50 of 250 nM, 50 nM, and 30 nM, respectively. Sunitinib inhibits the proliferation of MV4;11 and OC1-AML5 cells with IC50 of 8 nM and 14 nM, respectively, and induces apoptosis in a dose-dependent manner. [3]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human SW756 cell MYrHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? Moe5TY5pcWKrdHnvckBw\iCqdX3hckBUXzd3NjDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUG5MlE{PTFizszN MYnTRW5ITVJ?
human EoL-1-cell cell NUT6fmo3T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NGHm[FJKdmirYnn0bY9vKG:oIHj1cYFvKEWxTD2xMYNmdGxiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLk[0[U0xPg>? Mk\CV2FPT0WU
human MV-4-11 cell Ml62S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NHPhcphKdmirYnn0bY9vKG:oIHj1cYFvKE2YLUStNVEh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0xNjJ5MjDuUS=> MUTTRW5ITVJ?
human MV411 cells NYriVFU3WHKxbHnm[ZJifGmxbjDhd5NigQ>? MkK5OFghcA>? NYfQeVYxSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDNWlQyOSClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBq[zVyPUOgcm0> NV3EdpFvOjR7MES5OlE>
3T3 cells Mn\5SpVv[3Srb36gZZN{[Xl? Mm\XTY5pcWKrdHnvckBw\iCSRFfGMYlv\HWlZXSgRpJlXSCrbnPvdpBwemG2aX;uJIlvKDOWMzDj[YxteyC5aYToJFAvOSViYn;2bY5mKHOncoXtJIFt[nWvaX6sJGlEPTB;NzDuUS=> MVOxNlY1PjBzOR?=
HEK293 cells NEHvb25HfW6ldHnvckBie3OjeR?= Mn;hRolv\GmwZzDh[oZqdmm2eTD0c{BHVFR|IHPheIFtgXSrYzDkc41icW5iZYjwdoV{e2WmIHnuJGhGUzJ7MzDj[YxteyCkeTDjc41x\XSrdHn2[UBjcW6maX7nJIF{e2G7LDDL[F0xNjR5IH7N NUjFenFsOTl5NUSxPVk>
human MDA-MB-435 cells NXLqbXdKS3m2b4TvfIlkyqCjc4PhfS=> NGW5O|AzKGh? M1i0WWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1FSS2PQj20N|Uh[2WubIOsJGlEPTB;OT63JI5O Mln5NlQ5QTB4NUK=
human RS4-11 cells M4rSN2Z2dmO2aX;uJIF{e2G7 M3LkSWlvcGmkaYTpc44hd2ZiRlzUN{BifXSxcHjvd5Bpd3K7bHH0bY9vKGmwIHj1cYFvKFKVND2xNUBk\WyuczDh[pRmeiB{IHjyd{BjgSCnbHXjeJJw[2inbXnseY1qdmW|Y3XuZ4Uh[XO|YYmsJGlEPTB;OT65JI5O MmHONVk3PTR2MEi=
HUVEC NUS1U|NZS3m2b4TvfIlkyqCjc4PhfS=> NHr5XHVEgXSxdH;4bYNqfHliYXfhbY5{fCCKVW\FR{whUUN3ME2xNU45KG6P MnTRNlQ5QTB4NUK=
human Kasumi-1 cells MV7GeY5kfGmxbjDhd5NigQ>? NHLoW4NKdmirYnn0bY9vKG:oIHOtT4l1KGG3dH;wbI9{eGixconsZZRqd25iaX6gbJVu[W5iS3HzeY1qNTFiY3XscJMh[nliV3XzeIVzdiCkbH;0JIFv[Wy7c3nzMEBKSzVyPUG1JI5O MUKyNFg{OzB|OR?=
human NOS-1 cell Mnv6S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NGPDcmJKdmirYnn0bY9vKG:oIHj1cYFvKE6RUz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVUvOyCwTR?= NGHu[I9USU6JRWK=
mouse triple negative 4T1 cells NXvxWHhvS3m2b4TvfIlkyqCjc4PhfS=> MnPER5l1d3SxeHnjbZR6KGGpYXnud5QhdW:3c3WgeJJqeGynIH7l[4F1cX[nIETUNUBk\WyuczygTWM2OD1zNjDuUS=> MlHsNlQ5QTB4NUK=
human RS4-11 cells MlvVSpVv[3Srb36gZZN{[Xl? NIDuWYRKdmirYnn0bY9vKG:oIF\MWFMh[XW2b4Doc5NxcG:{eXzheIlwdiCrbjDoeY1idiCUU{StNVEh[2WubIOgZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m|LDDJR|UxRTF4IH7N MmTSNlA5OzNyM{m=
human MOLM13 cells MWjDfZRwfG:6aXRCpIF{e2G7 NV\ofIh2S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVU:OTUGzJINmdGy|IHHzd4V{e2WmIHHzJINmdGxidnnhZoltcXS7IHHmeIVzKDR6IHjyd{BjgSCPVGSgZZN{[XluIFnDOVA:OTdwNzDuUS=> M4XzfFI2ODh7OEGw
human U251 cells MVjGeY5kfGmxbjDhd5NigQ>? M2mxc2lvcGmkaYTpc44hd2ZiVlXHSnIzKGmwIHj1cYFvKFV{NUGgZ4VtdHNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCNCCLQ{WwQVE5Njlibl2= NYTi[o46OjR7MEC4OlU>
NIH3T3 cells Ml;TSpVv[3Srb36gZZN{[Xl? Mm\ONUBp M{nkV2lvcGmkaYTvdpkh[2:wY3XueJJifGmxbjDh[4FqdnO2IHj1cYFvKEuGUjDrbY5ie2ViZYjwdoV{e2WmIHnuJG5KUDOWMzDj[YxteyC5aYToJFQhfU1iQnnveIlvNUGqeD3BSWVGYU[ITF\BMYFucWSnIHH0JIFu[mmnboSgeIVueGW{YYT1doUh\m:{IEGgbJI> MWqxOlE3OjByOB?=
MDA-MB-231 cells MXzDfZRwfG:6aXRCpIF{e2G7 NIqxUJNEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckB1emmybHWgcoVo[XSrdnWgUWRCNU2ELUKzNUBk\WyuczygTWM2OD1{Mj6zJI5O M1jv[FI1QDlyNkWy
MCF7 cells Mne1R5l1d3SxeHnjxsBie3OjeR?= NHvGRXdEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBGWi2yb4PpeIl3\SCPQ1[3JINmdGy|LDDJR|UxRTJ5LkGgcm0> M4TUdlI1QDlyNkWy
human CGTH-W-1 cell NFz3NIRIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NHL0PXhKdmirYnn0bY9vKG:oIHj1cYFvKEOJVFitW{0yKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OzBwOUSgcm0> NGfpN|BUSU6JRWK=
human MONO-MAC-6 cell M13MWGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MVzJcohq[mm2aX;uJI9nKGi3bXHuJG1QVk9vTVHDMVYh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{Oy56IH7N MoW0V2FPT0WU
human HL60 cells NX7scIR6S3m2b4TvfIlkyqCjc4PhfS=> MUW0PEBp MVfDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUFYxKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHygeoli[mmuaYT5JIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;M{[uPEBvVQ>? NVOxZ2QzOjVyOEm4NVA>
human TT cells MVjQdo9tcW[ncnH0bY9vKGG|c3H5 M3LBOVczKGh? NUDRV2hFSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDUWEBk\WyuczDwdoV1emWjdHXkJIZweiB5MjDodpMh\m:ubH;3[YQh[nliY3;tdI92dmRvd3HzbI92fCCvZXHzeZJm\CCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVQxKG6P MU[yOFkxPDl4MR?=
human THP1 cells NYjjVXozS3m2b4TvfIlkyqCjc4PhfS=> MnrLOFghcA>? Mn\sR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gWGhROSClZXzsd{Bie3Onc4Pl[EBieyClZXzsJJZq[WKrbHn0fUBi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUS1Mlchdk1? NEi0eYczPTB6OUixNC=>
3T3 cells MWrGeY5kfGmxbjDhd5NigQ>? M{ThT2lvcGmkaYTpc44hd2ZiVnHzZ5Vt[XJiZX7kc5Rp\WyrYXyg[5Jwf3SqIH\hZ5RweiC{ZXPldJRweiCrbjCzWFMh[2WubIOsJGlEPTB;NUCgcm0> MlLTNVI3PDZyMUm=
human ALL-PO cell NFfLOmhIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MofWTY5pcWKrdHnvckBw\iCqdX3hckBCVExvUF:gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME23PU45QSCwTR?= Ml2yV2FPT0WU
human SH-SY5Y cells MlfTSpVv[3Srb36gZZN{[Xl? M4jxW2lvcGmkaYTpc44hd2ZiUFTHSnJj\XSjIHnuJIh2dWGwIGPIMXN[PVliY3XscJMh[nlicHjvd5Bpd3S7cn;zbY5mKEWOSWPBJIF{e2G7LDDJR|UxRTh|LkGgcm0> NVTNd5J4OjR6OUC2OVI>
human U251 cells MWXGeY5kfGmxbjDhd5NigQ>? NFPne5A3OCCvaX7z MnH4TY5pcWKrdHnvckBw\iCSRFfGVk1j\XSjIHnuJIh2dWGwIGWyOVEh[2WubIOgZ49ueG:3bnSgdJJmfHKnYYTl[EBnd3JiNkCgcYlvKGKnZn;y[UBRTEeILVLCJJN1cW23bHH0bY9vKG[xcjCxNEBucW6|IHL5JJBpd3OyaH;0fZJwe2mwZTDFUGlUSSCleYTvZoxwfCCvZYToc4QtKEmFNUC9PFMvOSCwTR?= NGP1fZQzPTh6MkWxPS=>
human NKM-1 cell MmDuS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MnP1TY5pcWKrdHnvckBw\iCqdX3hckBPU01vMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUm4MlUzKG6P NGHkNJFUSU6JRWK=
human HAEC cells M3jGXnBzd2yrZnXyZZRqd25iYYPzZZk> NUjaOFZuPzJiaB?= Mmn5RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCKQVXDJINmdGy|IHX4dJJme3OrbnegWmVITlJiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiSVO1NF0xNjFizszN MoLjNlI1PDR4N{m=
HUVEC cell M3XITWZ2dmO2aX;uJIF{e2G7 MYKyOEBp M4PF[GlvcGmkaYTpc44hd2ZiVlXHSk1CKGmwZIXj[YQhUFWYRVOgZ4VtdCC|cILveZRqdmdiYX\0[ZIhOjRiaILzJIJ6KGGwZ3nv[4Vv\XOrczDhd5NigSxiSVO1NF0xNjF{IN88US=> MmDwNlE4PDF{NEm=
human A431 cells NUHyS|NTTnWwY4Tpc44h[XO|YYm= MkPnOlAhdWmwcx?= Mnq1TY5pcWKrdHnvckBw\iCHR1\SJIlvKGi3bXHuJGE1OzFiY3XscJMh[2:vcH;1coQheHKndILlZZRm\CCob4KgOlAhdWmwIHLl[o9z\SCHR1[gd5RqdXWuYYTpc44h\m:{IEGwJI1qdnNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCKGO7dH;icI91KG2ndHjv[EwhUUN3ME2xO|IvOSCwTR?= NYPFcVlNOjV6OEK1NVk>
Sf9 cells NUHrcVJ3TnWwY4Tpc44h[XO|YYm= M2rRUWlvcGmkaYTpc44hd2ZiR2PUMZRi\2enZDDWSWdHWiCneIDy[ZN{\WRiaX6gV4Y6KGOnbHzzMEBKSzVyPUCuNVg2KM7:TR?= MYKxPVg2PDB3MR?=
human HT-29 cells M4LpNnBzd2yrZnXyZZRqd25iYYPzZZk> NWjVRZRlPzJiaB?= NEj1N5JCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjUMVI6KGOnbHzzJIV5eHKnc4PpcochXkWJRmKgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3Ojef-8kEBKSzVyPUCuN|Mh|ryP Mnf3NlI1PDR4N{m=
human KM12 cell MXLHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MnvETY5pcWKrdHnvckBw\iCqdX3hckBMVTF{IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD6zOVAyPCEQvF2= MkjBV2FPT0WU
human TE-15 cell MmD0S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MorZTY5pcWKrdHnvckBw\iCqdX3hckBVTS1zNTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuOVA4PjFizszN MmXDV2FPT0WU
human 697 cell M1Pm[Gdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M3ew[mlvcGmkaYTpc44hd2ZiaIXtZY4hPjl5IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD62NVQzPSEQvF2= NITIcoFUSU6JRWK=
human CAKI-1 cells M2TJNnBzd2yrZnXyZZRqd25iYYPzZZk> MYDBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEODS1mtNUBk\WyuczDh[pRmeiB2ODDodpMh[nliU2LCJIF{e2G7LDDHTVUxRTBwNkOg{txO MoLFNlI2PjB4Mke=
human MOLT-16 cell Mo[zS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NGjvSIVKdmirYnn0bY9vKG:oIHj1cYFvKE2RTGStNVYh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0xNjZ|MUOyJO69VQ>? NYLYfWV7W0GQR1XS
human GB-1 cell NGHudoNIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M1n1VmlvcGmkaYTpc44hd2ZiaIXtZY4hT0JvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuO|ExOjNizszN MYTTRW5ITVJ?
human TE-12 cell NHvwbXVIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M4KxVGlvcGmkaYTpc44hd2ZiaIXtZY4hXEVvMUKgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlgxPDV3IN88US=> NFPufo9USU6JRWK=
human NCI-H3122 cells NIOybWRRem:uaX\ldoF1cW:wIHHzd4F6 NXzlcGdqPzJiaB?= MUHBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE6FST3IN|EzOiClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUCuPFMh|ryP MnfWNlQ6ODR7NkG=
human ES6 cell NVPuSWtrT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NYrpOFJ5UW6qaXLpeIlwdiCxZjDoeY1idiCHU{[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlk5OTB4IN88US=> NWjJRVRjW0GQR1XS
human NCI-H526 cells NWjlS5Y1WHKxbHnm[ZJifGmxbjDhd5NigQ>? Mk\yO|IhcA>? MmL2RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCQQ1mtTFUzPiClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUGuNFEh|ryP MUiyOFkxPDl4MR?=
human LC-2-ad cell M1\QVmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NX7UTGxPUW6qaXLpeIlwdiCxZjDoeY1idiCOQz2yMYFlKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OS5zMUSwO{DPxE1? MlzKV2FPT0WU
human BL-70 cell MVLHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MYDJcohq[mm2aX;uJI9nKGi3bXHuJGJNNTdyIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT6xNVg1PiEQvF2= NH\XU5RUSU6JRWK=
human ETK-1 cell NEjO[FRIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NIfTdWtKdmirYnn0bY9vKG:oIHj1cYFvKEWWSz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NU4zQDV6IN88US=> MXHTRW5ITVJ?
human SW620 cells NGfNS5BRem:uaX\ldoF1cW:wIHHzd4F6 M1vIWFQ5KGh? NEW5V5pCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIGPXOlIxKGOnbHzzJIFnfGW{IES4JIhzeyCkeTDTVmIh[XO|YYmsJGdKPTB;MT6zJO69VQ>? Mle3NlI2PjB4Mke=
IM9 cells NVPMO|JZS3m2b4TvfIlkyqCjc4PhfS=> MnSzR5l1d3SxeHnjbZR6KGGpYXnud5QhUG:vbzDzZZBq\W6|IDjoeY1idiliSV25JINmdGy|IHHzd4V{e2WmIHHzJIdzd3e2aDDpcohq[mm2aX;uJIJ6KE2WVDDhd5NigSxiSVO1NF0yNjN3IN88US=> MU\TRW5ITVJ?
human A4-Fuk cell M4T1WGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MV\Jcohq[mm2aX;uJI9nKGi3bXHuJGE1NU[3azDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H589yNKEmFNUC9NU4{PDF2MTFOwG0> M{XCb3NCVkeHUh?=
human SR cell Mmf5S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MmHXTY5pcWKrdHnvckBw\iCqdX3hckBUWiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwNUS1O|Ih|ryP NV3vZnl6W0GQR1XS
human A3-KAW cell NGr1PG9Iem:5dHigbY5pcWKrdHnvckBie3OjeR?= NVLNbIxqUW6qaXLpeIlwdiCxZjDoeY1idiCDMz3LRXch[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiaXO1NF0yNjZ{NUS2JO69VQ>? MkPLV2FPT0WU
human KS-1 cell MkDaS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NGrOfFdKdmirYnn0bY9vKG:oIHj1cYFvKEuVLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlY6OjR5IN88US=> M3vzXXNCVkeHUh?=
human CTV-1 cell NHXO[IZIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NYn6[JFUUW6qaXLpeIlwdiCxZjDoeY1idiCFVG[tNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEvPzJ5NUGg{txO MnHHV2FPT0WU
human LB1047-RCC cell M1i5e2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M3i5dmlvcGmkaYTpc44hd2ZiaIXtZY4hVEJzMES3MXJESyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwOEG2NlQh|ryP M{K3e3NCVkeHUh?=
human MEG-01 cell MoHyS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MkW2TY5pcWKrdHnvckBw\iCqdX3hckBOTUdvMEGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlg{PTZ|IN88US=> MYnTRW5ITVJ?
human TE-11 cell Mn;RS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MmPxTY5pcWKrdHnvckBw\iCqdX3hckBVTS1zMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuPFM6QDVizszN NUj5[XJZW0GQR1XS
human CMK cell NVz1eYEyT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M1P0[GlvcGmkaYTpc44hd2ZiaIXtZY4hS02NIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT65OVUyPyEQvF2= M4LFO3NCVkeHUh?=
human NB1 cell NHi1bXlIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NFrzWmZKdmirYnn0bY9vKG:oIHj1cYFvKE6EMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuPVYyOTdizszN NFrL[W5USU6JRWK=
human MDA-MB-435 cells NInxeItRem:uaX\ldoF1cW:wIHHzd4F6 M1\DfFQ5KGh? MnvkRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCPRFGtUWIuPDN3IHPlcIx{KGGodHXyJFQ5KGi{czDifUBUWkJiYYPzZZktKEeLPUKg{txO NIq2Z5QzOjV4ME[yOy=>
human MCF7 cells MlvkVJJwdGmoZYLheIlwdiCjc4PhfS=> MXO0PEBp M4fkbGFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTVPGO{Bk\WyuczDh[pRmeiB2ODDodpMh[nliU2LCJIF{e2G7LDDHTVUxRTJizszN NEDuZ|UzOjV4ME[yOy=>
human A549 cells M2O4PWN6fG:2b4jpZ:Kh[XO|YYm= M3ixW|czKGh? NXfNNYtJS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTV2OTDj[YxteyCjc4Pld5Nm\CCjczDndo94fGhiaX7obYJqfGmxbjDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G7LDDJR|UxRTJwNESg{txO Ml\5NlM3ODJ2NEG=

他の多くの細胞株試験データをご覧になる場合はこちらをクリックして下さい

体内試験 Consistent with the substantial and selective inhibition of VEGFR2 or PDGFR phosphorylation and signaling in vivo, Sunitinib (20-80 mg/kg/day) exhibits broad and potent dose-dependent anti-tumor activity against a variety of tumor xenograft models including HT-29, A431, Colo205, H-460, SF763T, C6, A375, or MDA-MB-435. Sunitinib dosing at 80 mg/kg/day for 21 days leads to complete tumor regression in six of eight mice, without tumor re-growing during a 110-day observation period after the end of treatment. Second round of treatment with Sunitinib remains efficacious against tumors that are not fully regressed during the first round of treatment. Sunitinib treatment results in significant decrease in tumor MVD, with ~40% reduction in SF763T glioma tumors. SU11248 treatment results in a complete inhibition of additional tumor growth of luciferase-expressing PC-3M xenografts, despite no reduction in tumor size. [2] Sunitinib treatment (20 mg/kg/day) dramatically suppresses the growth subcutaneous MV4;11 (FLT3-ITD) xenografts and prolongs survival in the FLT3-ITD bone marrow engraftment model. [3]

お薦めの試験操作(参考用のみ)

キナーゼ試験:

[1]

+ 展開

Biochemical Tyrosine Kinase Assays:

IC50 values for Sunitinib against VEGFR2 (Flk-1) and PDGFRβ are determined using glutathione S-transferase fusion proteins containing the complete cytoplasmic domain of the RTK. Biochemical tyrosine kinase assays to quantitate the trans-phosphorylation activity of VEGFR2 (Flk-1) and PDGFRβ are performed in 96-well microtiter plates precoated (20 μg/well in PBS; incubated overnight at 4 °C) with the peptide substrate poly-Glu,Tyr (4:1). Excess protein binding sites are blocked with the addition of 1-5% (w/v) BSA in PBS. Purified GST-fusion proteins are produced in baculovirus-infected insect cells. GST-VEGFR2 and GST-PDGFRβ are then added to the microtiter wells in 2 × concentration kinase dilution buffer consisting of 100 mM HEPES, 50 mM NaCl, 40 μM NaVO4, and 0.02% (w/v) BSA. The final enzyme concentration for GST-VEGFR2 or GST-PDGFRβ is 50 ng/mL. Twenty-five μL of diluted Sunitinib are subsequently added to each reaction well to produce a range of inhibitor concentrations appropriate for each enzyme. The kinase reaction is initiated by the addition of different concentrations of ATP in a solution of MnCl2 so that the final ATP concentrations spanned the Km for the enzyme, and the final concentration of MnCl2 is 10 mM. The plates are incubated for 5-15 minutes at room temperature before stopping the reaction with the addition of EDTA. The plates are then washed three times with TBST. Rabbit polyclonal antiphosphotyrosine antisera are added to the wells at a 1:10,000 dilution in TBST containing 0.5% (w/v) BSA, 0.025% (w/v) nonfat dry milk, and 100 μM NaVO4 and incubated for 1 hour at 37 °C. The plates are then washed three times with TBST, followed by the addition of goat antirabbit antisera conjugated with horseradish peroxidase (1:10,000 dilution in TBST). The plates are incubated for 1 hour at 37 °C and then washed three times with TBST. The amount of phosphotyrosine in each well is quantitated after the addition of 2,2′-azino-di-[3-ethylbenzthiazoline sulfonate] as substrate.
細胞試験:

[3]

+ 展開
  • 細胞株: RS4;11, MV4;11, and OC1-AML5
  • 濃度: Dissolved in DMSO, final concentrations ~10 μM
  • 反応時間: 24 and 48 hours
  • 実験の流れ:

    Cells are starved overnight in medium containing 0.1% FBS prior to addition of Sunitinib and FL (50 ng/mL; FLT3-WT cells only). Proliferation is measured after 48 hours of culture using the Alamar Blue assay or trypan blue cell viability assays. Apoptosis is measured 24 hours after Sunitinib addition by Western blotting to detect cleavage of poly (ADP-ribose) polymerase (PARP) or levels of caspase-3.


    (参考用のみ)
動物試験:

[2]

+ 展開
  • 動物モデル: Female nu/nu mice implanted s.c. with HT-29, A431, Colo205, H-460, SF763T, C6, A375, or MDA-MB-435, and male nu/nu mice bearing luciferase-expressing PC-3M tumors
  • 製剤: Formulated as a carboxymethyl cellulose suspension or as a citrate buffered (pH 3.5) solution
  • 投薬量: ~80 mg/kg
  • 投与方法: Orally once daily
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 25 mg/mL (62.73 mM) warming
Water Insoluble
Ethanol Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます(文献ではなく、Selleckの実験によるデータ):
5% DMSO+corn oil
混合させたのち直ちに使用することを推奨します。
7mg/mL

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。

化学情報

分子量 398.47
化学式

C22H27FN4O2

CAS No. 557795-19-4
保管
in solvent
別名 SU11248

便利ツール

モル濃度計算器

モル濃度計算器

求めたい質量、体積または濃度を計算してください。

質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • 質量
    濃度
    体積
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備するために必要な希釈率を計算してください。Selleck希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 入力 出力 )

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2

モル濃度計算器

質量 濃度 体積 分子量

臨床試験

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03729245 Not yet recruiting Renal Cell Carcinoma|Metastatic Renal Cell Carcinoma Nektar Therapeutics|Bristol-Myers Squibb December 2018 Phase 3
NCT03673501 Not yet recruiting Gastrointestinal Stromal Tumors Deciphera Pharmaceuticals LLC December 2018 Phase 3
NCT03641326 Not yet recruiting Gliosarcoma|Central Nervous System Sarcoma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) November 20 2018 Phase 2
NCT03323710 Suspended Renal Cell Carcinoma Military Institute of Medicine Poland September 2018 Phase 2
NCT03025893 Recruiting Glioblastoma Multiforme|Glioblastoma Adult|Glioblastoma|Recurrent Brain Tumor|GBM VU University Medical Center August 31 2018 Phase 2|Phase 3
NCT03275558 Withdrawn Recurrent Glioblastoma|Gliosarcoma|Anaplastic Gliomas Center Trials & Treatment July 17 2018 Phase 1

技術サポート

ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

  • * 必須

PDGFRシグナル伝達経路

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